Echchannaoui Hakim, Bianchi Matteo, Baud David, Bobst Martine, Stehle Jean-Christophe, Nardelli-Haefliger Denise
Institute of Microbiology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, CH1011 Lausanne, Switzerland.
Infect Immun. 2008 May;76(5):1940-51. doi: 10.1128/IAI.01484-07. Epub 2008 Mar 10.
Cervical cancer, the second leading cause of cancer deaths in women, is the consequence of high-risk human papillomavirus (HPV) infections. Toward the development of therapeutic vaccines that can induce both innate and adaptive mucosal immune responses, we analyzed intravaginal (ivag) vaccine delivery of live attenuated Salmonella enterica serovar Typhimurium expressing HPV16L1 as a model antigen. Innate immune responses were examined in cervicovaginal tissues by determining gene expression patterns by microarray analysis using nylon membranes imprinted with cDNA fragments coding for inflammation-associated genes. At 24 h, a wide range of genes, including those for chemokines and Th1- and Th2-type cytokine and chemokine receptors were up-regulated in mice ivag immunized with Salmonella compared to control mice. However, the majority of transcripts returned to their steady-state levels 1 week after immunization, suggesting a transient inflammatory response. Indeed, cervicovaginal histology of immunized mice showed a massive, but transient, infiltration of macrophages and neutrophils, while T cells were still increased after 7 days. Ivag immunization also induced humoral and antitumor immune responses, i.e., serum and vaginal anti-HPV16VLP antibody titers similar to those induced by oral immunization, and significant protection in tumor protection experiments using HPV16-expressing C3 tumor cells. These results show that ivag immunization with live attenuated Salmonella expressing HPV16 antigens modulates the local mucosal gene expression pattern into a transient proinflammatory profile, elicits strong systemic and mucosal immunity against HPV16, and confers protection against HPV16 tumor cells subcutaneously implanted in mice. Examination of the efficacy with which ivag HPV16E7E6 Salmonella induces regression of tumors located in cervicovaginal tissue is warranted.
宫颈癌是女性癌症死亡的第二大主要原因,是高危型人乳头瘤病毒(HPV)感染的结果。为了开发能够诱导先天性和适应性黏膜免疫反应的治疗性疫苗,我们分析了以表达HPV16L1作为模型抗原的减毒活鼠伤寒沙门氏菌进行阴道内(ivag)疫苗递送的情况。通过使用印有编码炎症相关基因的cDNA片段的尼龙膜进行微阵列分析来确定基因表达模式,从而在宫颈阴道组织中检测先天性免疫反应。与对照小鼠相比,在24小时时,用沙门氏菌进行阴道内免疫的小鼠中,包括趋化因子、Th1型和Th2型细胞因子及趋化因子受体等多种基因上调。然而,免疫后1周,大多数转录本恢复到稳态水平,表明存在短暂的炎症反应。实际上,免疫小鼠的宫颈阴道组织学显示巨噬细胞和中性粒细胞大量但短暂浸润,而7天后T细胞仍增加。阴道内免疫还诱导了体液和抗肿瘤免疫反应,即血清和阴道抗HPV16VLP抗体滴度与口服免疫诱导的滴度相似,并且在使用表达HPV16的C3肿瘤细胞的肿瘤保护实验中具有显著的保护作用。这些结果表明,用表达HPV16抗原的减毒活沙门氏菌进行阴道内免疫可将局部黏膜基因表达模式调节为短暂的促炎状态,引发针对HPV16的强大全身和黏膜免疫,并对皮下植入小鼠的HPV16肿瘤细胞提供保护。有必要检查阴道内HPV16E7E6沙门氏菌诱导宫颈阴道组织中肿瘤消退的疗效。